Immature urine

Ileum, intricLsic factor, 61 Immature urine, 113 Immune system, SO-53 infant. 134-135 iron-ccKntaining enzymes, 747 zinc deficiency and, 815 Immunization, enteric, 136 Immunoglobulin A (IgA), in mother s milk, 134... 

The determinants of F. have been subject to experimentation mostly in field and captive studies of ungulates. These support the expected association between the frequency and occurrence of Flehmen and the seasonality of reproduction. The elicitation of F. can also depend upon the social context presentation of urine or other stimuli alone may not produce consistent displays. When conspecific urine was tested out of context (i.e. no female present) in male Black-tailed deer, there was no discrimination between urine from individual adult males or between urine from estrous/non-estrous females (Altieri, 1980). Correlation of male endocrine status in reindeer (Rangifer tarandus) showed that the elevation of testosterone during rut and the duration of F. elicited by female urine was coincident F. bouts during rat were twice as long following exposure to adult female urine as to that of immature females (Mossing and Damber, 1981). 

Another study by McChesney and co-workers on the metabolism of nalidixic acid in the immature calf(23) demonstrated a pattern of metabolism very different than in man. The half-life of nalidixic acid was found to be about 24 hours and a large amount was excreted into the feces. The immature calves were also unable to excrete nalidixic acid into the urine at concentrations greater than found in the plasma and conjugated drug was present at low levels only. Calves seven months old had metabolic patterns much closer to man the plasma half-life was about 1.5 hours, the concentration of excretion into the urine was at least ten times that in plasma and the extent of conjugation was increased. The inability to metabolize nalidixic acid by the immature calf was considered to be due to incomplete development of its metabolic system. 

The concentrations of 16 constituents of male mouse urine vary with the male s dominance status. Dihydrofurans, ketones, and acetates decreased in subordinates. Two sesquiterpene compounds, a- and /3-farnesene, are elevated in dominants urine 1 week after establishing dominance. The bladder or voided urine of dominants contains more 2-5ec-butyl-4,5-dihydrothiazole. Four compounds depend on hormones a- and /5-farnesene, dehydro-exo-brevicomin, and 2-5cc -butyl-4,5-dihydrothiazole. The latter two are absent in urine of immature or castrated males, and testosterone treatment restores their presence. In addition, a-and /3-farnesene do not occur in urine of immature males and are merely reduced in urine of castrates. They are not found in bladder urine and originate in the preputial glands (Harvey etal., 1989). While subordinate male mice have reduced levels of farnesenes, levels of their major urinary proteins remain high (Malone etal, 2001). 

The kidney normally manufactures erythropoietin, the growth factor for the production of red blood cells. In fact, erythropoietin was first isolated from the urine of patients with anemia, a condition characterized by too few red blood cells. Red cells carry oxygen to the body s tissues, and if too little oxygen is delivered to them, certain kidney cells produce erythropoietin. Most of this substance goes into the blood, where it circulates to the bone marrow and other tissues and triggers increased production of red cells from immature cells. Some erythropoietin spills into the urine. The concentration of erythropoietin in the blood is very low. The concentration is even lower in urine, but urine is easy, safe, and cheap to collect, and it does not contain a large number of other proteins. 

Mechanism of Action An antiretroviral that is rapidly converted to amprenavir, which inhibits HIV-1 protease by binding to the enzyme s active site, thus preventingthe processing of viral precursors and resulting in the formation of immature, noninfectious viral particles. Therapeutic Effect Impairs HIV replication and proliferation. Pharmacokinetics Rapidly absorbed after PO administration. Protein binding 90%. Metabolized in the liver. Excreted in urine and feces. Half-life 7.7 hr. 

There are two pyridoxal phosphate-requiring enzymes in the homocysteine degradation pathway, which are associated with genetic diseases. In homo-cystinuria, cystathionine synthase is defective, and large amounts of homocystine are excreted in the urine. Some homocystinurics respond to the administration of large doses of vitamin B6. In cystathioninuria, cystathionase is either defective or absent. These patients excrete cystathionine in the urine. Cystathionase is often underactive in the newborns with immature livers, and cysteine and cystine become essential amino acids. Human milk protein is especially rich in cysteine, presumably to prepare the newborn for such a contingency. 

No evidence was found (Dl) for immaturity of the enzyme systems involved in tryptophan metabolism, since kynurenine and xanthurenic acid could be detected in the first weeks of life in urine of infants loaded with tryptophan. 

Proximal tubular function is immature, and bicarbonate and glucose reabsorption is reduced. This leads to a low serum bicarbonate concentration. Glycosuria and aminoaciduria may be found in the normal neonate. A baby s ability to concentrate urine is poor. A urine osmolality of 600 mmol/kg is the maximum that can be produced. In the neonatal period, the kidney s ability to excrete water and electrolytes is limited. Thus, great care must be taken in the provision of intravenous fluids. 

Indinavir (800 mg/t.i.d.) is an inhibitor of the HIV protease, which is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV. Indinavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature noninfectious viral particles. Cross-resistance between indinavir and HIV reverse-transcriptase inhibitors is unlikely because the enzyme targets involved are different. Cross-resistance was noted between indinavir and the protease inhibitor ritonavir. Varying degrees of cross-resistance have been noted between indinavir and other HIV protease inhibitors. Indinavir is metabolized in the liver, and seven metabolites have been identified, and 20% of indinavir is excreted unchanged in the urine. 

Until recently, extensive use of conventional physico-chemical methods such as gas chromatography and mass spectroscopy that are commonly applied to odorants have not revealed significant characteristics distinguishing urinary constituents of MHC-congenic mice. (One report indicated a difference only in immature females (Schwende, Jorgenson and Novotny 1984). Major reasons for this difficulty are (a) the vast number of different volatile compounds found in urine and (b) the (assumed) fact that the distinctive odors are attributable to pattern of several or many volatile compounds. Under this latter assumption it is the distinctive pattern that is characteristic, and disturbance of this pattern of compound odorants (Boyse et al. 1991b) by typical chemical separation procedures would likely destroy odortype information. 

Another clear example of stereotypic behavior that is at least partially under che-mosensory control is the 70-kHz vocalization that male house mice emit when exposed to the odor of female urine, but not of male urine. However, odors from estrous, anestrous, and immature females are similarly effective, and males do not vocalize unless they make... 

Secondary sex hormone isolated frbi urine. Leaflets or prismatic needljsi EtOH or Me CO. M.p. 178° (184-5 Sol, prae. all org. solvents. Very H2O, [ot] 1 94 6° in EtOH, -f 1C 3 MeOH. Produces male sex characteri immature animals. Physiologically doses of 150-200 y on ButenaMt (cap< i test and 60 y on Tschopp (seminal vei... 

The histidinemic urine is sometimes only weakly positive or negative on ferric chloride testing, which reflects either the instability of imidazole-pyruvic acid, the relation of its excretion to protein intake, immaturity of histidine transaminase, or a combination of these factors. Even after histidine loading, histidinemic neonates excrete much smaller quantities of imi-dazolepyruvic acid than do older children. In patients with urocanase deficiency, the levels of blood histidine and urine imidazolepyruvic acid are normal or slightly elevated. Therefore, it is necessary to do a quantitative analysis of blood histidine and urine ferric chloride test in order to overlook the patients with this condition. 

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